Myocardial Water Content Research Articles

T2 mapping post acute myocardial infarction: a novel technique in assessing myocardial edema

ObjectiveCardiovascular magnetic resonance (CMR) is considered the gold standard imaging modality for assessing myocardial infarction lesions, offering precise myocardial tissue characterization. Elevated transverse relaxation time (T2) serves as a specific indicator of increased myocardial water content, thus becoming a valuable index for myocardial edema. However, conventional T2-weighted CMR sequence exhibits several limitations, primarily providing qualitative information. In contrast, recently developed quantitative T2 mapping techniques overcome these limitations, enabling a more reliable assessment of myocardial edema. These techniques offer the advantage of diagnosing and monitoring myocardial injury without the necessity of contrast agents. Our study aims to add to a growing literature demonstrating the efficacy of quantitative T2 mapping technique to detect and quantify regions of myocardial edema post-myocardial infarction.ResultNative T1 and T2 mapping accurately identified myocardial edema in all patients enrolled in the study. Notably, native T1 and T2 values exhibited a significant elevation in the infarcted myocardium compared to the remote myocardium (for T1: 1295.50 ± 87.65 vs. 1074.95 ± 92.86 ms, respectively; and for T2: 74.63 ± 6.51 vs. 52.53 ± 6.26 ms, respectively; p < 0.0001 for both). Microvascular obstruction was observed in 12 out of 20 patients, affecting one or more myocardial segments within the infarct areas. Among this subgroup, regions with a microvascular obstruction within the infarct zone displayed lower T1 and T2 values compared to areas of infarction without microvascular obstruction (for T1: 1115.05 ± 64.70 vs. 1295.50 ± 87.65 ms, respectively; and for T2: 53.65 ± 3.56 vs. 74.63 ± 6.51 ms, respectively; p < 0.0001 for both). Additionally, we provided reference values for myocardial T1 and T2 specific to our facility’s 1.5 Tesla CMR system, applicable to both infarct and remote myocardium.ConclusionParametric T1 and T2 mapping techniques can detect and quantify myocardial edema resulting from myocardial infarction. The presence of microvascular obstruction that results from revascularization injury affects both T1 and T2 values. This information can be used and has broad clinical implications for diagnosis and guiding or monitoring the treatment of myocardial infarction.

Abstract 128: Saline Load Induces Acute Changes In Ventricular Extracellular Volume And Mass

Background: Maladaptive left ventricular hypertrophy (LVH) in hypertension is generally regarded as a result of myocardial fibrosis. However, salt loading induces a systemic and isotonic expansion of the extracellular (EC) volume in tissues, which could affect myocardial structure independent of fibrosis. Methods: Cardiac MRI, including cine-images and native T1 and T2 mapping as surrogates for EC volume and myocardial water content, was performed immediately before and after a saline infusion test (SIT; 2L NaCL 0.9% in 4h) in patients with primary aldosteronism (PA), a prototypic sodium-retentive form of hypertension. Results: We enrolled 13 consecutive patients with PA (5F; 50±12 yo; BP=140/88±14/7 mmHg; sK + =3.7±0.4 mmol/L on KCl supplements; renin=2.5[2.0-4.8] mIU/L, aldosterone=568[368-737] pmol/L), lacking aldosterone suppression after SIT (562 [262-776] pmol/L, p=0.127). SIT induced a small but significant increase in wall thickness (septum: 9.0±1.5 vs 9.5±1.0 mm, p=0.027) and, overall, in left ventricular mass (56.3±9.1 vs 58.0±9.2 g/m 2 , p=0.026), paralleled by an increase in myocardial T1 (1012±29 vs 1027±25 ms, p&lt;0.001) and T2 (49.9±2.0 vs 51.2±2.7 ms, p=0.012). After saline the left ventricular ejection fraction was mildly reduced (56[55-62] vs 53[51-59]%, p=0.023), reflecting an increase in end-systolic (ES) volume (38±10 vs 43±10 ml/m 2 , p=0.030) without significant changes in the end-diastolic (ED) volume (88±18 vs 91±16 ml/m 2 , p=0.114). Conclusions: Within a timeframe inconsistent with EC matrix remodeling, saline load induced an increase in ventricular mass and an expansion of the EC volume, i.e. edema, in a human model of salt-related disease.

Exercise-induced myocardial T1 increase and right ventricular dysfunction in recreational cyclists: a CMR study

PurposeAlthough cardiac troponin I (cTnI) increase following strenuous exercise has been observed, the development of exercise-induced myocardial edema remains unclear. Cardiac magnetic resonance (CMR) native T1/T2 mapping is sensitive to the pathological increase of myocardial water content. Therefore, we evaluated exercise-induced acute myocardial changes in recreational cyclists by incorporating biomarkers, echocardiography and CMR.MethodsNineteen male recreational participants (age: 48 ± 5 years) cycled the ‘L’étape du tour de France” (EDT) 2021’ (175 km, 3600 altimeters). One week before the race, a maximal graded cycling test was conducted to determine individual heart rate (HR) training zones. One day before and 3–6 h post-exercise 3 T CMR and echocardiography were performed to assess myocardial native T1/T2 relaxation times and cardiac function, and blood samples were collected. All participants were asked to cycle 2 h around their anaerobic gas exchange threshold (HR zone 4).ResultsEighteen participants completed the EDT stage in 537 ± 58 min, including 154 ± 61 min of cycling time in HR zone 4. Post-race right ventricular (RV) dysfunction with reduced strain and increased volumes (p < 0.05) and borderline significant left ventricular global longitudinal strain reduction (p = 0.05) were observed. Post-exercise cTnI (0.75 ± 5.1 ng/l to 69.9 ± 41.6 ng/l; p < 0.001) and T1 relaxation times (1133 ± 48 ms to 1182 ± 46 ms, p < 0.001) increased significantly with no significant change in T2 (p = 0.474). cTnI release correlated with increase in T1 relaxation time (p = 0.002; r = 0.703), post-race RV dysfunction (p < 0.05; r = 0.562) and longer cycling in HR zone 4 (p < 0.05; r = 0.607).ConclusionStrenuous exercise causes early post-race cTnI increase, increased T1 relaxation time and RV dysfunction in recreational cyclists, which showed interdependent correlation. The long-term clinical significance of these changes needs further investigation.Trial registration numbers and dateNCT 04940650 06/18/2021. NCT 05138003 06/18/2021.

Native T2 Predicts Myocardial Inflammation Irrespective of a Patient's Volume Status.

Myocardial inflammation and edema are major pathological features in myocarditis. Myocardial tissue water content and myocardial edema can be quantified via T2 mapping. Thus, cardiac magnetic resonance (CMR) is the noninvasive gold standard for diagnosing myocarditis. Several studies showed an impact of short-term volume changes on T2 relaxation time. Plasma volume status (PVS) is a good surrogate parameter to quantify a patient's volume status, and it is simple to use. The aim of this study was to determine the effect of PVS on the diagnostic value of T2 relaxation time in myocardial inflammation. Between April 2017 and December 2022, patients who were indicated for cardiac CMR were included in our prospective clinical registry. Patients with myocardial inflammation and those with unremarkable findings were analyzed in the present study. A blood sample was drawn, and PVS was calculated. Patients were separated into PVS tertiles to explore a possible nonlinear dose-response relationship. Logistic regression analysis was used to determine whether T2 is an independent predictor of myocardial inflammation. A total of 700 patients (47.43% female) were eligible for analysis. Of these, 551 patients were healthy (78.7%), while 149 (21.3%) showed signs of myocardial inflammation. The T2 relaxation time was elevated in patients with myocardial inflammation (40 ms [IQR 37-42 ms] vs. 38.0 ms [IQR 36-39 ms], p < 0.001). PVS showed no difference between the groups (-12.94 [IQR -18.4--7.28] vs.-12.19 [IQR -18.93--5.87], p = 0.384). T2 showed a clear dose-response relationship with PVS, with increasing T2 values along the PVS tertiles. In spite of this, T2 was found to be an independent marker of myocardial inflammation in logistic regression (OR T2 1.3 [95% CI 1.21-1.39], p < 0.001), even after adjusting for PVS (OR T2 [adj. PVS] 1.31 [95% CI 1.22-1.40], p < 0.001). Despite a dose-response relationship between T2 and the volume status, T2 was found to be an independent indicator of myocardial inflammation.

Myocardial oedema contributes to interstitial expansion and associates with mechanical and electrocardiographic changes in takotsubo syndrome: a CMR T1 and T2 mapping study.

myocardial oedema is largely represented in takotsubo syndrome (TTS) and may contribute to alter the myocardium morphology and function. The aim of the study is to describe relationships between oedema, mechanical, and electrical abnormalities in TTS. the study included n = 32 hospitalized TTS patients and n = 23 controls. Cardiac magnetic resonance (CMR) with tissue mapping and feature tracking was performed with concomitant 12-lead electrocardiogram (ECG) recording. Mean age of TTS was 72 ± 12 years old, 94% women. Compared with controls, patients had higher left ventricular (LV) mass, worse systolic function, higher septal native T1 (1116 ± 73 msec vs. 970 ± 23 msec, P < 0.001), T2 (56 ± 5 msec vs. 46 ± 2 msec, P < 0.001), and extracellular volume (ECV) fraction (32 ± 5% vs. 24 ± 1%, P < 0.001). TTS patients had higher apicobasal gradient of T2 values (12 ± 6 msec vs. 2 ± 6 msec, P < 0.001); basal LV wall displayed higher native T1, T2, and ECV (all P < 0.002) but similar circumferential strain against controls (-23 ± 3% vs. -24 ± 4%, P = 0.351). In the TTS cohort, septal T2 values showed significant correlations with native T1 (r = 0.609, P < 0.001), ECV (r = 0.689, P < 0.001), left ventricular ejection fraction (r = -0.459, P = 0.008) and aVR voltage (r = -0.478, P = 0.009). Negative T-wave voltage and QTc length correlated with apicobasal T2 mapping gradient (r = 0.499, P = 0.007 and r = 0.372, P = 0.047, respectively) but not with other tissue mapping measurements. CMR T1 and T2 mapping demonstrated increased myocardial water content conditioning interstitial expansion in acute TTS, detected even outside areas of abnormal wall motion. Oedema burden and distribution associated with mechanical and electrocardiographic changes, making it a potential prognostic marker and therapeutic target in TTS.

66 MYOCARDIAL EDEMA CONTRIBUTES TO INTERSTITIAL EXPANSION AND ASSOCIATES WITH MECHANICAL AND ELECTROCARDIOGRAPHIC CHANGES IN TAKOTSUBO SYNDROME: A CMR T1 AND T2 MAPPING STUDY

Abstract Background myocardial edema has a central role in takotsubo syndrome (TTS). Relationships between edema, mechanical and electrical abnormalities in TTS are still elusive. Methods n=32 hospitalized TTS patients and n=23 controls were analyzed. We performed cardiac magnetic resonance (CMR) with tissue mapping for the assessment of edema and interstitial expansion, global longitudinal (GLS) and circumferential strain (GCS) were evaluated by CMR feature-tracking. Twelve-lead ECGs were recorded at the time of CMR in TTS patients, aVR voltage, negative T-wave voltage and QTc length were calculated. Results mean age of the TTS cohort was 72±12-year-old, 94% women, undergoing CMR at a median of 4 days (interquartile range 2, 6) after hospital admission. Compared with controls, patients had increased LV mass (55±11 g/m2 vs 46±8 g/m2, p&amp;lt;0.001), worse left ventricular ejection fraction (LVEF), GLS and GCS (all p&amp;lt;0.001), higher septal native T1 (1116±73 msec vs 970±23 msec, p&amp;lt;0.001), T2 (56±5 msec vs 46±2 msec, p&amp;lt;0.001) and extra-cellular volume (ECV) fraction (32±5% vs 24±1%, p&amp;lt;0.001). TTS patients had higher apicobasal gradient of T2 values (12±6 msec vs 2±6 msec, p&amp;lt;0.001), basal LV wall displayed higher native T1, T2 and ECV (all p&amp;lt;0.002) but similar circumferential strain against controls (-23±3% vs -24±4%, p=0.351). In the TTS cohort, septal T2 value showed significant correlations with native T1 (r=0.609, p&amp;lt;0.001), ECV (r=0.689, p&amp;lt;0.001), LVEF (r=-0.459, p=0.008) and aVR voltage (r=-0.437, p&amp;lt;0.05). Negative T waves voltage and QTc length significantly correlated with apicobasal T2 mapping gradient (r=0.499, p=0.007 and r=0.372, p=0.047 respectively) but not with other tissue mapping measurements. Conclusions CMR T1 and T2 mapping demonstrated increased myocardial water content conditioning interstitial expansion in acute TTS. Myocardial edema was detected even outside areas of abnormal wall motion, its burden and distribution associated with mechanical and electrocardiographic changes, making it a potential prognostic marker and therapeutic target in TTS.

Myocardial Edema Provides a Link Between Pulmonary Arterial Hypertension and Pericardial Effusion.

Myocardial Edema Provides a Link Between Pulmonary Arterial Hypertension and Pericardial Effusion.

Clinical assessment of adenosine stress and rest cardiac magnetic resonance T1 mapping for detecting ischemic and infarcted myocardium

Cardiac magnetic resonance (CMR) spin-lattice relaxation time (T1) may be influenced by pathologic conditions due to changes in myocardial water content. We aimed to validate the principle and investigate T1 mapping at rest and adenosine stress to differentiate ischemic and infarcted myocardium from controls. Patients with suspected coronary artery disease who underwent CMR were prospectively recruited. Native rest and adenosine stress T1 maps were obtained using standard modified Look-Locker Inversion-Recovery technique. Among 181 patients included, T1 values were measured from three groups. In the control group, 72 patients showed myocardium with a T1 profile of 1,039 ± 75 ms at rest and a significant increase during stress (4.79 ± 3.14%, p < 0.001). While the ischemic (51 patients) and infarcted (58 patients) groups showed elevated resting T1 compared to controls (1,040 ± 90 ms for ischemic; 1,239 ± 121 ms for infarcted, p < 0.001), neither of which presented significant T1 reactivity (1.38 ± 3.02% for ischemic; 1.55 ± 5.25% for infarcted). We concluded that adenosine stress and rest T1 mapping may be useful to differentiate normal, ischemic and infarcted myocardium.

Influence of hydration status on cardiovascular magnetic resonance myocardial T1 and T2 relaxation time assessment: an intraindividual study in healthy subjects

BackgroundMyocardial native T1 and T2 relaxation time mapping are sensitive to pathological increase of myocardial water content (e.g. myocardial edema). However, the influence of physiological hydration changes as a possible confounder of relaxation time assessment has not been studied. The purpose of this study was to evaluate, whether changes in myocardial water content due to dehydration and hydration might alter myocardial relaxation times in healthy subjects.MethodsA total of 36 cardiovascular magnetic resonance (CMR) scans were performed in 12 healthy subjects (5 men, 25.8 ± 3.2 years). Subjects underwent three successive CMR scans: (1) baseline scan, (2) dehydration scan after 12 h of fasting (no food or water), (3) hydration scan after hydration. CMR scans were performed for the assessment of myocardial native T1 and T2 relaxation times and cardiac function. For multiple comparisons, repeated measures ANOVA or the Friedman test was used.ResultsThere was no change in systolic blood pressure or left ventricular ejection fraction between CMR scans (P > 0.05, respectively). T1 relaxation times were significantly reduced with dehydration (987 ± 27 ms [baseline] vs. 968 ± 29 ms [dehydration] vs. 986 ± 28 ms [hydration]; P = 0.006). Similar results were observed for T2 relaxation times (52.9 ± 1.8 ms [baseline] vs. 51.5 ± 2.0 ms [dehydration] vs. 52.2 ± 1.9 ms [hydration]; P = 0.020).ConclusionsDehydration may lead to significant alterations in relaxation times and thereby may influence precise, repeatable and comparable assessment of native T1 and T2 relaxation times. Hydration status should be recognized as new potential confounder of native T1 and T2 relaxation time assessment in clinical routine.

R2 prime (R2') magnetic resonance imaging for post-myocardial infarction intramyocardial haemorrhage quantification.

To assess whether R2* is more accurate than T2* for the detection of intramyocardial haemorrhage (IMH) and to evaluate whether T2' (or R2') is less affected by oedema than T2* (R2*), and thus more suitable for the accurate identification of post-myocardial infarction (MI) IMH. Reperfused anterior MI was performed in 20 pigs, which were sacrificed at 120 min, 24 h, 4 days, and 7 days. At each time point, cardiac magnetic resonance (CMR) T2- and T2*-mapping scans were recorded, and myocardial tissue samples were collected to quantify IMH and myocardial water content. After normalization by the number of red blood cells in remote tissue, histological IMH increased 5.2-fold, 10.7-fold, and 4.1-fold at Days 1, 4, and 7, respectively. The presence of IMH was correlated more strongly with R2* (r = 0.69; P = 0.013) than with T2* (r = -0.50; P = 0.085). The correlation with IMH was even stronger for R2' (r = 0.72; P = 0.008). For myocardial oedema, the correlation was stronger for R2* (r = -0.63; P = 0.029) than for R2' (r = -0.50; P = 0.100). Multivariate linear regressions confirmed that R2* values were significantly explained by both IMH and oedema, whereas R2' values were mostly explained by histological IMH (P = 0.024) and were little influenced by myocardial oedema (P = 0.262). Using CMR mapping with histological validation in a pig model of reperfused MI, R2'more accurately detected IMH and was less influenced by oedema than R2* (and T2*). Further studies are needed to elucidate whether R2' is also better suited for the characterization of post-MI IMH in the clinical setting.

P5278Myocardial abnormalities in people living with Human Immunodeficiency Virus (PLWH) detected using cardiovascular magnetic resonance (CMR)

Abstract Background Antiretroviral therapy (ART) has dramatically improved the prognosis in PLWH with survival nearing that of HIV negative people. PLWH may develop significant comorbidities as they age including cardiovascular disease (CVD) such as myocardial infarction, sudden cardiac death, heart failure, as well as subclinical evidence of myocardial inflammation. Overall, ART treated patients are at an increased CVD risk with some studies quoting a 2.2 fold relative risk. Aim To assess the incidence of functional, structural and tissue characterisation changes in PLWH using CMR with multiparametric mapping Methods 39 PLWH (34 men, mean age 55.8±10.9, mean duration of HIV 17.8±9.29 years) and 29 healthy volunteers (20 men, mean age 45.1±8.3) underwent CMR with late gadolinium enhancement (LGE) imaging, T1 and T2 mapping. Results Of PLWH, only 7 scans (18%) were normal. LV ejection fraction was significantly lower and LV mass significantly higher compared to controls. Native T1, a marker of diffuse fibrosis or increased myocardial water content was no different between the groups. T2, a more specific marker of myocardial oedema, was elevated in PLWH. Sixteen PLWH (41%) had evidence of LGE including 8 with an ischaemic pattern (7 sub-endocardial and one transmural) and 8 with a non-ischaemic pattern (5 with mid-wall enhancement and 3 with RV insertion point LGE. No controls had evidence of LGE. Student t-Test: PLWH versus controls PLWH (n=39) Control (n=29) P-value LVEF (%) 59±15 67±5 &lt;0.01 iLVM 79±24 56±13 &lt;0.01 Native T1 (ms) 1021±52 1001±41 0.116 T2 (ms) 48±2 46±2 &lt;0.05 LGE 16 (41%) 0 (0%) &lt;0.001 LVEF (%) = Left Ventricular Ejection Fraction; iLVM = Indexed Left Ventricular Mass (g/m2); LGE = Late Gadolinium Enhancement. Conclusion This study identifies a number of cardiac changes associated with HIV and prolonged treatment with ART. The elevated LV mass may be associated with hypertension, commonly found in PLWH. The elevated myocardial T2 compared to controls may be due to chronic inflammation associated to prolonged HIV exposure. There was no evidence of diffuse fibrosis but focal areas of non-ischaemic scar were a common finding which may relate to previous myocarditis or HIV-related cardiomyopathy. A fifth of PLWH also had evidence of previous myocardial infarction. We propose to image asymptomatic PLWH to further classify, diagnose and treat a vulnerable group of patients who are now described as having a normal life expectancy.

Acute changes in cardiac structural and tissue characterisation parameters following haemodialysis measured using cardiovascular magnetic resonance

In patients with chronic kidney disease (CKD), reverse left ventricular (LV) remodelling, including reduction in LV mass, can be observed following long-term haemodialysis (HD) and has been attributed to regression of LV hypertrophy. However, LV mass can vary in response to changes in myocyte volume, edema, or fibrosis. The aims of this study were to investigate the acute changes in structural (myocardial mass and biventricular volumes) and tissue characterization parameters (native T1 and T2) following HD using cardiovascular magnetic resonance (CMR). Twenty-five stable HD patients underwent non-contrast CMR including volumetric assessment and native T1 and T2 mapping immediately pre- and post-HD. The mean time between the first and second scan was 9.1 ± 1.1 hours and mean time from completion of dialysis to the second scan was 3.5 ± 1.3 hours. Post-HD, there was reduction in LV mass (pre-dialysis 98.9 ± 36.9 g/m2 vs post-dialysis 93.3 ± 35.8 g/m2, p = 0.003), which correlated with change in body weight (r = 0.717, p < 0.001). Both native T1 and T2 reduced significantly following HD (Native T1: pre-dialysis 1085 ± 43 ms, post-dialysis 1072 ± 43 ms; T2: pre-dialysis 53.3 ± 3.0 ms, post-dialysis 51.8 ± 3.1 ms, both p < 0.05). These changes presumably reflect acute reduction in myocardial water content rather than regression of LV hypertrophy. CMR with multiparametric mapping is a promising tool to assess the cardiac changes associated with HD.

The involvement of AQP1 in myocardial edema induced by pressure overload in mice.

To investigate the effect of aquaporin-1 (AQP1) on heart edema induced by transverse aortic constriction (TAC) in mice, and to explore whether inhibiting the expression of AQP1 could attenuate myocardial edema and improve cardiac function. The C57BL/6 mice were divided into four groups: (1) the sham group; 2) the sham + acetazolamide group: mice were orally gavaged with acetazolamide (20 mg/kg/day) after sham operation; (3) the TAC group: a mouse model of pressure overload induced by TAC for two weeks; (4) the TAC + acetazolamide group: mice were orally gavaged with acetazolamide (20 mg/kg/day) after TAC. Cardiac function was detected by echocardiography after 2 weeks' TAC. The ratio of heart weight to body weight (HW/BW) and myocardial water content were calculated. The mRNA and protein expressions of AQP1 were measured by reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot, respectively. Significant myocardial hypertrophy and dysfunction were found in TAC mice. The ratio of HW/BW, myocardial water content, and the mRNA and protein expression of AQP1 of the TAC group were markedly higher than those of the sham group. By contrast, acetazolamide administration reduced the ratio of HW/BW and myocardial water content, whereas improved cardiac dysfunction induced by TAC. Moreover, acetazolamide reduced the mRNA and protein expression of AQP1 in TAC mice. The expression of AQP1 was closely related to myocardial edema induced by TAC. The inhibition of AQP1 could reduce myocardial edema and improve cardiac dysfunction.

Role of cardiac T1 mapping and extracellular volume in the assessment of myocardial infarction.

Although late gadolinium enhancement on cardiac magnetic resonance imaging remains the reference standard for scar assessment, it does not provide quantitative information about the extent of pathophysiological changes within the scar tissue. T1 mapping and extracellular volume (ECV) mapping are steadily becoming diagnostic and prognostically useful tests for in vivo myocardial histology, influencing clinical decision-making. Quantitative native T1 maps (acquired without a contrast agent) represent the longitudinal relaxation time within the myocardium and changes with myocardial extracellular water (edema, focal, or diffuse fibrosis), fat, iron, and amyloid protein content. Post-contrast ECV maps estimate the size of the extracellular space and have sensitivity in the identification of interstitial disease. Both pre- and post-contrast T1 mapping are emerging as comprehensive tools for the assessment of numerous conditions including ischemic scarring that occurs post myocardial infarction (MI). This review outlines the current evidence and potential future role of T1 mapping in MI. We conclude by highlighting some of the remaining challenges such as quality control, standardization of image acquisition for clinical practice, and automated methods for quantifying infarct size, area at risk, and myocardial salvage post MI.

Three-Dimensional Self-Navigated T2 Mapping for the Detection of Acute Cellular Rejection After Orthotopic Heart Transplantation.

BackgroundT2 mapping is a magnetic resonance imaging technique measuring T2 relaxation time, which increases with the myocardial tissue water content. Myocardial edema is a component of acute cellular rejection (ACR) after heart transplantation. This pilot study compares in heart transplantation recipients a novel high resolution 3-dimensional (3D) T2-mapping technique with standard 2-dimensional (2D) T2-mapping for ACR detection.MethodsConsecutive asymptomatic patients (n = 26) underwent both 3D T2 mapping and reference 2D T2 mapping magnetic resonance imaging on the day of endomyocardial biopsy (EMB). 3D T2 maps were obtained at an isotropic spatial resolution of 1.72 mm (voxel volume 5.1 mm3). 2D and 3D maps were matched anatomically, and maximum segmental T2 values were compared blinded to EMB results. In addition, all 3D T2 maps were rendered as 3D images and inspected for foci of T2 elevation.ResultsT2 values of segments from 2D and reformatted 3D T2 maps agreed (p > 0.5). The highest 2D segmental T2 values were 49.9 ± 4.0 ms (no ACR = 0R, n = 18), 48.9 ± 0.8 ms (mild ACR = 1R, n = 3), and 65.0 ms (moderate ACR = 2R). Rendered 3D T2 maps of cases with 1R showed foci with significantly elevated T2 signal (T2 = 58.2 ± 3.6 ms); 5 cases (28%) in the 0R group showed foci with increased T2 values (>2 SD above adjacent tissue) that were not visible on the 2D T2 maps.ConclusionsThis pilot study in a small cohort suggests equivalency of standard segmental analysis between 3D and 2D T2-mapping. 3D T2 mapping provides a spatial resolution that permits detection of foci with elevated T2 in patients with mild ACR.

Global myocardial oedema in advanced decompensated heart failure.

To use cardiac magnetic resonance (CMR) imaging with quantitative T2 mapping as surrogate for myocardial water content in patients with advanced decompensated heart failure (ADHF), compare these values with T2-values observed in chronic heart failure, and evaluate the change with decongestive therapy. Volumetric CMR measurements and quantitative T2 mapping were performed in 18 consecutive ADHF patients with clinical signs of volume overload. Eleven patients with stable heart failure were used as controls. Vasodilator therapy and diuretics were administered to achieve a pulmonary arterial wedge pressure (PAWP) of <18 mmHg and central venous pressure (CVP) of <12 mmHg, after which CMR was repeated. ADHF patients (62 ± 12 years; 89% male; left ventricular ejection fraction 23 ± 8%) presented with low cardiac index (2.08 ± 0.59 L/min/m2), high PAWP (25 ± 7 mmHg), and high CVP (14 ± 5 mmHg). After decongestion, the patients had a significant increase in cardiac index (+0.41 ± 0.53 L/min/m2; P = 0.005) and decreases in both PAWP (-9 ± 6 mmHg; P < 0.001) and CVP (-6 ± 5 mmHg; P < 0.001). At baseline, global left ventricular T2-values were higher in ADHF patients compared with controls (59.5 ± 4.6 vs. 54.7 ± 2.2 ms, respectively; P = 0.001). After decongestion, T2-values fell significantly to 55.9 ± 5.1 ms (P = 0.001), comparable with controls (P = 0.580). In contrast, psoas muscle T2-values were similar at baseline (38.6 ± 4.4 ms) vs. after decongestion (37.8 ± 4.8 ms; P = 0.397). Each 1 ms decrease in global left ventricular T2-value during decongestion was associated with a 1.14 ± 0.40 mmHg decrease in PAWP (P = 0.013), after correction for age and gender. Patients presenting with ADHF and volume overload have increased global left ventricular-but not psoas muscle-T2-values, which decrease with successful decongestion. Relief of myocardial oedema correlates with haemodynamic unloading.

Adenosine Stress and Rest T1 Mapping Can Differentiate Between Ischemic, Infarcted, Remote, and Normal Myocardium Without the Need for Gadolinium Contrast Agents

ObjectivesThe aim of this study was to evaluate the potential of T1 mapping at rest and during adenosine stress as a novel method for ischemia detection without the use of gadolinium contrast. BackgroundIn chronic coronary artery disease (CAD), accurate detection of ischemia is important because targeted revascularization improves clinical outcomes. Myocardial blood volume (MBV) may be a more comprehensive marker of ischemia than myocardial blood flow. T1 mapping using cardiac magnetic resonance (CMR) is highly sensitive to changes in myocardial water content, including MBV. We propose that T1 mapping at rest and during adenosine vasodilatory stress can detect MBV changes in normal and diseased myocardium in CAD. MethodsTwenty normal controls (10 at 1.5-T; 10 at 3.0-T) and 10 CAD patients (1.5-T) underwent conventional CMR to assess for left ventricular function (cine), infarction (late gadolinium enhancement [LGE]) and ischemia (myocardial perfusion reserve index [MPRI] on first-pass perfusion imaging during adenosine stress). These were compared to novel pre-contrast stress/rest T1 mapping using the Shortened Modified Look-Locker Inversion recovery technique, which is heart rate independent. T1 values were derived for normal myocardium in controls and for infarcted, ischemic, and remote myocardium in CAD patients. ResultsNormal myocardium in controls (normal wall motion, MPRI, no LGE) showed normal resting T1 (954 ± 19 ms at 1.5-T; 1,189 ± 34 ms at 3.0-T) and significant positive T1 reactivity during adenosine stress compared to baseline (6.2 ± 0.5% at 1.5-T; 6.3 ± 1.1% at 3.0-T; all p < 0.0001). Infarcted myocardium showed the highest resting T1 of all tissue classes (1,442 ± 84 ms), without significant T1 reactivity (0.2 ± 1.5%). Ischemic myocardium showed elevated resting T1 compared to normal (987 ± 17 ms; p < 0.001) without significant T1 reactivity (0.2 ± 0.8%). Remote myocardium, although having comparable resting T1 to normal (955 ± 17 ms; p = 0.92), showed blunted T1 reactivity (3.9 ± 0.6%; p < 0.001). ConclusionsT1 mapping at rest and during adenosine stress can differentiate between normal, infarcted, ischemic, and remote myocardium with distinctive T1 profiles. Stress/rest T1 mapping holds promise for ischemia detection without the need for gadolinium contrast.

Abstract 18331: Endothelial Microrna-155 Promotes Myocardial Microvascular Permeability and Inflammatory Cell Adhesion in Experimental Septic Cardiomyopathy

Introduction: Septic cardiomyopathy remains a leading cause of death in critically ill patients. Myocardial edema and inflammatory cell recruitment to cardiac interstitial space are proposed mechanisms underlying sepsis-induced contractile dysfunction. Hypothesis: Evaluate the role of endothelial microRNA-155 (miR-155) in experimental septic cardiomyopathy. Methods: Experimental sepsis was induced using LPS injection in WT (n=20) and miR-155-/- (KO; n=20) male mice. Cardiac function was evaluated through echocardiography. Expression of NOS2, NOS3, VASP phosphorylation and myocardial nitrite/nitrate content was evaluated. Cardiac microvascular (MV) permeability was assessed with evans blue-albumin conjugate leaking to extravascular space and myocardial water content. Mouse cardiac MV endothelial cells (MCMVEC; CD31+Sca-1+CD45-) were isolated with FACS. Quantification of miR-155, cytokine mRNA profile and adhesion molecules (ICAM1, VCAM1 and E-selectin) was performed. Human cardiac MV endothelial cells (HCMVEC) were transfected with anti-miR-155 or scramble LNA probe and incubated with LPS (100ng/mL) or vehicle for 24h. Evaluation of cytokine mRNA profile, NOS isoforms, VASP phosphorylation and adhesion molecules was performed. Monocyte adhesion assay was performed using Dil-stained THP1 monocytic cells. Results: LPS exposure increased miR-155 expression in the myocardium, MCMVEC and HCMVEC. KO mice presented with attenuated LPS-induced cardiac dysfunction, MV permeability, NOS2 expression and VASP phosphorylation, compared with WT. KO MCMVEC presented with attenuated LPS-induced cytokine expression and adhesion molecules, compared with WT cells. Mir-155 inhibition in HCMVEC prevented LPS-induced overexpression of cytokines and adhesion molecules, nitric oxide production and monocyte adhesion, through SOCS1-mediated inhibition of STAT3 and NF-kB signaling pathways. Conclusions: Endothelial miR-155 is upregulated in experimental septic cardiomyopathy. MiR-155 knockout attenuates LPS-induced myocardial dysfunction, edema and MV permeability. In MCMVEC and HCMVEC, miR-155 inhibition blunted LPS-induced nitric oxide production, cytokine and cell adhesion molecules overexpression.

Pathophysiology Underlying the Bimodal Edema Phenomenon After Myocardial Ischemia/Reperfusion

BackgroundPost-ischemia/reperfusion (I/R) myocardial edema was recently shown to follow a consistent bimodal pattern: an initial wave of edema appears on reperfusion and dissipates at 24 h, followed by a deferred wave that initiates days after infarction, peaking at 1 week. ObjectivesThis study examined the pathophysiology underlying this post-I/R bimodal edematous reaction. MethodsForty instrumented pigs were assigned to different myocardial infarction protocols. Edematous reaction was evaluated by water content quantification, serial cardiac magnetic resonance T2-mapping, and histology/immunohistochemistry. The association of reperfusion with the initial wave of edema was evaluated in pigs undergoing 40-min/80-min I/R and compared with pigs undergoing 120-min ischemia with no reperfusion. The role of tissue healing in the deferred wave of edema was evaluated by comparing pigs undergoing standard 40-min/7-day I/R with animals subjected to infarction without reperfusion (chronic 7-day coronary occlusion) or receiving post-I/R high-dose steroid therapy. ResultsCharacterization of post-I/R tissue changes revealed maximal interstitial edema early on reperfusion in the ischemic myocardium, with maximal content of neutrophils, macrophages, and collagen at 24 h, day 4, and day 7 post-I/R, respectively. Reperfused pigs had significantly higher myocardial water content at 120 min and T2 relaxation times on 120 min cardiac magnetic resonance than nonreperfused animals. Permanent coronary occlusion or high-dose steroid therapy significantly reduced myocardial water content on day 7 post-infarction. The dynamics of T2 relaxation times during the first post-infarction week were altered significantly in nonreperfused pigs compared with pigs undergoing regular I/R. ConclusionsThe 2 waves of the post-I/R edematous reaction are related to different pathophysiological phenomena. Although the first wave is secondary to reperfusion, the second wave occurs mainly because of tissue healing processes.

Severe aortic stenosis has blunted myocardial T1 relaxation response to vasodilator stress: a cardiac magnetic resonance adenosine stress test study

Background Aortic stenosis is characterized by impaired myocardial perfusion reserve due to coronary microvascular dysfunction. T1 mapping is sensitive to myocardial water content of both intra- and extracellular in origin, but the effect of intravascular compartment changes on T1 has never been assessed previously. We aimed to assess the effect of adenosine-induced vasodilatation on native (pre-contrast) T1 values in patients with severe aortic stenosis (AS) before and after aortic valve replacement (AVR).